Damage to the central nervous system following head injury frequently results in the destruction of neurons and the loss of the behavioral functions normally controlled by those cells. In many cases, there is little hope for full recovery, since neurons within the central nervous system show little capacity for regeneration. The long term goal of this research is to develop methods for the stimulation and promotion of neuronal reorganization and regeneration of those neurons that survive the traumatic insult. A number of studies have shown that the nervous system has a greater capacity for repair and functional reorganization when damaged during early development. Therefore, we have proposed to study the molecular factors that are necessary for the appropriate development of axons and dendrites of neurons in the central nervous system, with the aim of extending or reestablishing the period of functional reorganization. Three classes of molecules are known to be involved in the regulation of growth of neuronal processes: neuronotrophic factors, extracellular matrix molecules, and cell adhesion molecules. Although much information has been gained on the importance of these factors in the promotion of axonal growth from the projection neurons within the CNS, little is known about the role of these molecules in the growth of axons and dendrites from non-projection neurons. However, traumatic injury to the central nervous system typically involves damage to both gray and white matter. Therefore, we propose to address the following questions in tissue cultured neurons and glial cells: 1. Do the same factors that promote neurite outgrowth from projection neurons also promote neurite extension from local circuit neurons? 2. Do the same factors that promote axonal growth also promote dendritic growth? 3. Do glial cells isolated from different regions of the CNS differ in their ability to promote the growth of neurites from projection neurons vs. local circuit neurons? 4. Do glial cells isolated from different regions of the CNS differ in their ability to promote the growth of dendrites vs. axons?